Contribution of Ghrelin to the Pathogenesis of Growth Hormone Deficiency

In this review we described the interactions between ghrelin and the growth hormone (GH)-insulin-like growth factor 1 (IGF-1) axis in children and adults with growth hormone deficiency (GHD). A possible involvement of these interactions in the pathogenesis of unexplained cases of GHD was suggested. Current research provides more and more details to the knowledge on the circadian rhythm of ghrelin. We gathered reports on the decreasing effect of Helicobacter pylori-related chronic gastritis on the number of ghrelin immunopositive cells and the consequent decrease in ghrelin serum concentration. The gastrointestinal tract microflora modification of the ghrelin action, by the mechanism of molecular mimicry, was also stressed. Moreover, the mutual relationships between ghrelin and the TSH-FT4/FT3 axis in growth and metabolic processes are described. It is to be recalled that FT4 and FT3 exert a permissive impact on IGF-1 action and, in turn, GH, in reaction mediated by IGF-1, enhances the monodeiodination of FT4 to FT3. Finally, we discussed the latest attempts to use the GH secretagogue receptor (GHS-R) analogues for possible diagnostic and therapeutic purposes.

Automated summary

This review discussed the interactions between ghrelin and the GH-IGF-1 axis in individuals with GHD, suggesting their possible involvement in the pathogenesis of unexplained cases of GHD. It also highlighted the impact of Helicobacter pylori-related chronic gastritis on ghrelin levels and the modification of ghrelin action by gastrointestinal tract microflora. Additionally, the review described the mutual relationships between ghrelin and the TSH-FT4/FT3 axis in growth and metabolic processes, as well as the potential diagnostic and therapeutic applications of GH secretagogue receptor analogues.